ChemFaces is a professional high-purity natural products manufacturer.
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1. Reference standards
2. Pharmacological research
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More articles cited ChemFaces products.
Yakugaku Zasshi.2018 Jan 30;Industrial Crops and Products2017 Jan.Journal of Medicinal Plant Research.2013 Nov 7J Nat Prod. 2017 Apr 28;Sci Rep. 2017 Oct 11;
J. Int. J. of Food Properties 13 Feb 2017Experimental Parasitology2015 March 24.Food Chem.2018 Jun 30;Chemistry of Natural CompoundsJan. 2018;Phytochemistry Letters2015 June
BMC Complement Altern Med.2014 Sep 23;14:352.Biofactors.2017 Oct 24.Front Pharmacol. 2017 Sep 29;Tropical J. of Pha. ResearchNo 3 (2017)
Our products had been exported to the following research institutions and universities, And still growing.
Wroclaw Medical University (Poland)Research Unit Molecular Epigenet... (Germany)University of East Anglia (United Kingdom)Guangzhou Institutes of Biomedic... (China)
The Australian National University (Australia)Molecular Biology Institute of B... (Spain)Universidad Miguel Hernández (Spain)Universidade de Franca (Brazil)
Michigan State University (USA)VIB Department of Plant Systems ... (Belgium)University of Mysore (India)
|| Dihydrorotenone is a potent mitochondrial inhibitor and probably induces Parkinsonian syndrome. It induces human plasma cell apoptosis by provoking endoplasmic reticulum stress and induces cell death by activating the p38 but not the JNK signaling pathway.|
||p21 | p53 | Akt | ERK | JNK | p38MAPK|
|J Biochem Mol Toxicol. 2014 May;28(5):232-8. |
|Natural pesticide dihydrorotenone arrests human plasma cancer cells at the G0/G1 phase of the cell cycle.[Pubmed: 24615755]|
|Dihydrorotenone (DHR) is a natural pesticide used for farming including organic produces. We recently found that Dihydrorotenone induces human plasma cell apoptosis by provoking endoplasmic reticulum stress.|
METHODS AND RESULTS:
In the present study, we found that Dihydrorotenone arrested human plasma cancer cells at the G0/G1 phase of the cell cycle. Dihydrorotenone inhibited cyclin D2 transactivation, thus inhibiting its mRNA expression. In addition, Dihydrorotenone upregulated the cell cycle repressors p21 and p53. Dihydrorotenone also increased the phosphorylation level of p53, suggesting the upregulated transactivation function of p53, which was confirmed by the induction of p21, a substrate of activated p53. Moreover, Dihydrorotenone downregulated AKT and ERK phosphorylation, an incentive of cell cycle progression.
Therefore, these results collectively demonstrated that Dihydrorotenone disrupts the cell cycle progress, which suggests that Dihydrorotenone is toxic to human plasma cells. Caution is thus suggested when handling with this agent.
||The herbs of Derris trifoliata Lour.
||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
Recent ChemFaces New Products and Compounds
Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.PMID: 29328914
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.PMID: 29149595
Scientific Reports 2017 Dec 11;7(1):17332.doi: 10.1038/s41598-017-17427-6.PMID: 29230013
Molecules. 2017 Oct 27;22(11). pii: E1829.doi: 10.3390/molecules22111829.PMID: 29077044
J Cell Biochem. 2018 Feb;119(2):2231-2239.doi: 10.1002/jcb.26385. PMID: 28857247
Phytomedicine. 2018 Feb 1;40:37-47. doi:10.1016/j.phymed.2017.12.030PMID: 29496173
Calculate Dilution Ratios(Only for Reference)
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
|PLoS One. 2013 Jul 26;8(7):e69911. |
|The natural pesticide dihydrorotenone induces human plasma cell apoptosis by triggering endoplasmic reticulum stress and activating p38 signaling pathway.[Pubmed: 23922854]|
|Dihydrorotenone (DHR) is a natural pesticide widely used in farming industry, such as organic produces. Dihydrorotenone is a potent mitochondrial inhibitor and probably induces Parkinsonian syndrome, however, it is not known whether Dihydrorotenone is toxic to other systems. |
METHODS AND RESULTS:
In the present study, we evaluated the cytotoxicity of Dihydrorotenone on human plasma cells. As predicted, Dihydrorotenone impaired mitochondrial function by decreasing mitochondrial membrane potential in plasma cells. Because mito-dysfunction leads to unfolded protein response (UPR) and endoplasmic reticulum (ER) stress, we examined the signature proteins in ER stress, including GRP78, ATF4, and CHOP. After Dihydrorotenone treatment, these proteins were significantly upregulated. It is reported that activation of the mitogen-activated protein kinases p38 and JNK are involved in endoplasmic reticulum stress. However, in the subsequent study, Dihydrorotenone was found to activate p38 but not the JNK signaling. When pre-treated with p38 inhibitor SB203580, activation of p38 and cell apoptosis induced by Dihydrorotenone was partially blocked.
Thus, we found that Dihydrorotenoneinduced human plasma cell death by activating the p38 but not the JNK signaling pathway. Because plasma cells are very important in the immune system, this study provided a new insight in the safety evaluation of Dihydrorotenone application.